Early Memory Formation Disrupted by Atypical PKC Inhibitor ZIP in the Medial Prefrontal Cortex But Not Hippocampus

被引：21

作者：

Evuarherhe, Obaro ^{[1
]}

Barker, Gareth R. I. ^{[1
]}

Savalli, Giorgia ^{[2
]}

Warburton, Elizabeth C. ^{[1
]}

Brown, Malcolm W. ^{[1
]}

机构：

[1] Univ Bristol, Dept Physiol & Pharmacol, Sch Med Sci, Bristol BS8 1TD, Avon, England

[2] Med Univ Vienna, Dept Neurophysiol & Neuropharmacol, A-1090 Vienna, Austria

来源：

HIPPOCAMPUS | 2014年 / 24卷 / 08期

基金：

英国生物技术与生命科学研究理事会; 英国惠康基金;

关键词：

recognition memory; hippocampus; medial prefrontal cortex; encoding; maintenance; KINASE M-ZETA; OBJECT-LOCATION; RECOGNITION; CONSOLIDATION; TRAFFICKING; ACQUISITION; PLASTICITY; PLACE;

D O I：

10.1002/hipo.22281

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Atypical isoforms of protein kinase C (aPKCs; particularly protein kinase M zeta: PKM zeta) have been hypothesized to be necessary and sufficient for the maintenance of long-term potentiation (LTP) and long term memory by maintaining postsynaptic AMPA receptors via the GluA2 subunit. A myristoylated PKM zeta pseudosubstrate peptide (ZIP) blocks PKM zeta activity. We examined the actions of ZIP in medial prefrontal cortex (mPFC) and hippocampus in associative recognition memory in rats during early memory formation and memory maintenance. ZIP infusion in either hippocampus or mPFC impaired memory maintenance. However, early memory formation was impaired by ZIP in mPFC but not hippocampus; and blocking GluA2-dependent removal of AMPA receptors did not affect this impairment caused by ZIP in the mPFC. The findings indicate: (i) a difference in the actions of ZIP in hippocampus and medial prefrontal cortex, and (ii) a GluA2-independent target of ZIP (possibly PKC lambda) in the mPFC during early memory formation. (C) 2014 Wiley Periodicals, Inc.

引用

页码：934 / 942

页数：9

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